EARLY EXPOSURE TO ANTIDEPRESSANTS AFFECT ADULT ANXIETY
About 15 percent of
women in the United States suffer from anxiety disorders and depression during
their pregnancies, and many are prescribed antidepressants. However little is
known about how early exposure to these medications might affect their offspring
as they mature into adults.
The answer to that
question is vital, as 5 percent of all babies born in the U.S. -- more than
200,000 a year -- are exposed to antidepressants during gestation via
transmission from their mothers.
Now, a UCLA team has
studied early developmental exposure to two different antidepressants, Prozac
and Lexapro, in a mouse model that mimics human third trimester medication
exposure. They found that, although these serotonin-selective reuptake
inhibiting antidepressants (SSRIs) were thought to work the same way, they did
not produce the same long-term changes in anxiety behavior in the adult mice.
The mice exposed to
Lexapro had permanent changes in serotonin neurotransmission and were less
anxious as adults than the mice exposed to Prozac, said study senior author
Anne M. Andrews, professor of psychiatry and chemistry and biochemistry and the
Richard Metzner Endowed Chair in Clinical Neuropharmacology at the Semel
Institute for Neuroscience & Human Behavior and California NanoSystems
Institute.
"This was quite
surprising, since these medications belong to the same drug class and are
believed to work by the same mechanism. The implications of these findings are
that with additional investigation, it may be possible to identify specific
antidepressants that are safer for pregnant women," Andrews said.
"It's important to recognize that major depressive disorders and anxiety
disorders are serious medical conditions that often require therapeutic intervention.
Prescribing the safest medication for mother and child is paramount."
The results of the
six-year study appear early online Dec. 19, 2014 in the peer-reviewed journal Neuropsychopharmacology.
SSRIs like Prozac and
Lexapro act by blocking the actions of a protein called the serotonin
transporter, which removes the neurotransmitter serotonin from the signaling
space between neurons. Andrews and her team also studied mice that had been
genetically engineered to have a reduction or absence of serotonin transporters
in the brain. They were able to compare early antidepressant exposure to
permanent reductions in serotonin transporter function.
Genetic reductions in
serotonin transporters are thought to be a risk factor, particularly when
combined with stressful life experiences, for developing anxiety and mood
disorders. And in fact, the genetically engineered mice Andrews studied showed
more anxiety as adults.
"It might be
possible that when mothers are treated for depression or anxiety during
pregnancy that certain SSRIs may promote resilience to developing these
disorders in children later in life," Andrews said. "However, it will
take much more research for us to understand whether this is true and whether
certain SSRIs may be better at promoting these effects."
Going forward, Andrews
and her team plan to investigate the effects of early exposure to
antidepressants on the architectures of serotonin neurons. Based on the current
findings, they suspect that early exposure to Lexapro may alter the way
serotonin neurons innervate brain regions involved in mood and anxiety
behavior. They also plan to investigate other SSRIs such as Paxil and Zoloft.
"Current
antidepressant therapies are ineffective in treating anxiety and depression in
large numbers of patients, and advances in predicting individual responses are
hindered by difficulties associated with characterizing complex influences of
genetic and environmental factors on serotonergic transmission in humans,"
the study states. "Highly controlled animal models, such as those studied
here, represent avenues by which to identify factors potentially influencing
behavioral domains associated with emotion-related disorders."
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